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In the past 30 years, the field of pain management has increasingly incorporated technologies of neurostimulation as part of the treatment algorithm for patients with intractable pain. These technologies include peripheral nerve stimulation, spinal cord stimulation, deep brain stimulation, sacral nerve stimulation, and trigeminal nerve stimulation. More and more patients with complex pain conditions who have failed more conservative management are finding some degree of relief through the use of these devices.

The inspiration for development of these technologies came from the landmark “gate control theory” introduced by Melzack and Wall in 1965.1 Although this model fails to explain certain phenomena seen in painful conditions and cannot account for all of the observed effects of neurostimulation, the gate control theory remains the primary paradigm used to describe how neurostimulation acts to modify pain transmission. The gate control theory is based on the presence of cells in the dorsal horn of the spinal cord that receive afferent signals from peripheral C fibers conveying painful stimuli, as well as non-nociceptive sensory fibers. Once pain signals reach these dorsal horn interneurons, a “gate” is activated and painful impulses propagate along ascending fibers to the brain, resulting in conscious awareness of pain. Wall and Melzack proposed that the gate could be closed to the transmission of painful impulses through the selective activation of non-nociceptive fibers. Thus, the notion of using neurostimulatory devices to preferentially activate non-nociceptive fibers as a means of diminishing pain was born.

The application of neurostimulation has been increasing since C. Norman Shealy implanted the first spinal cord stimulator device in 1967. The scope of conditions amenable to these technologies has likewise expanded as they have become more widely used in varying populations of patients around the world. Current indications for the use of these devices include isolated peripheral nerve injuries, failed back surgery syndrome, peripheral vascular disease with critical limb ischemia, refractory angina pectoris, deafferentation syndromes, spinal-cord-injury–related pain, interstitial cystitis, and trigeminal neuralgia. Other applications are continuously being evaluated, including the use of spinal cord stimulation as a means to monitor evoked potentials during thoracoabdominal aneurysm repair.2

Although the gate control theory seems to explain the primary mechanism by which neurostimulation works, it cannot account for some of the clinically observed effects of spinal cord stimulation. Some researchers have proposed that spinal cord stimulation inhibits transmission of painful impulses partly by inducing a differential conduction block of afferent nociceptive fibers via antidromic stimulation. That the effects of stimulation can outlast the duration of the stimulation would seem, however, to indicate this is not the only mechanism by which neurostimulation influences pain transmission. A number of investigators have speculated that neurohumoral mechanisms are also involved. Studies have been conducted to further elucidate which mediators may contribute. Substances that have been purported to be involved in the neuromodulatory effects of spinal cord stimulation include endogenous opioids, gamma (γ)-aminobutyric acid (GABA), adenosine, substance P, serotonin, calcitonin gene-related peptide (CGRP), ...

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